Various types of pacing leads have been developed for endocardial introduction into different chambers of a patient's heart, typically the right ventricle or right atrial appendage, as well as the coronary sinus. These flexible leads usually are constructed having an outer polymeric sheath encasing one or more electrical conductors. One conductor is typically attached at its distal end to the shank portion of a tip electrode. In bipolar or multipolar leads, one or more further conductors are provided in coaxial or co-linear relation to the first conductor and are connected at their distal end to a more proximally located, ring-shaped electrode situated along the lead body. The proximal ends of each conductor are each coupled to a connector, which includes a single pin in unipolar leads, and additional pins or in-line rings in bipolar and multipolar leads.
These pacing leads can be attached to a variety of pacing devices such as a single chamber atrial pacemaker (AAI), a single chamber ventricular pacemaker (VVI), or a dual chamber pacemaker (DDD). In a conventional AAI or VVI pacemaker, only one lead is required. Stimulation in the AAI pacemakers is normally performed with the lead located in the right atrium. Stimulation with a VVI pacemaker normally takes place in the apex of the right ventricle. The conventional DDD pacemaker requires two leads. Similar to AAI pacing, one of the DDD pacemaker leads is placed in the heart's right atrium and similar to VVI pacing another DDD pacemaker lead is placed in the apex of the right ventricle. The leads are used to sense electrical activity in the heart and to deliver stimulation pulses when spontaneous electrical activity ceases. The leads are often shaped so the atrial lead and the ventricular lead are adapted to conform to their desired placement in the heart when the electrode system is implanted. In a DDD lead system, the implantation of dual curved leads has proven difficult due to the complicated nature of implanting two curved leads into two separate chambers of the heart.
In a healthy heart an electrical impulse starts at the sinoatrial (SA) node located in the upper right of the right atrium and travels to the right and left atria through the myocyte cells, depolarizing the cells and causing them to contract together. This action generally takes about 0.04 seconds. The electrical impulse then travels to the atrioventricular node (AV node) located in the lower left side of the right atrium. A natural delay occurs which allows the atria to contract and the ventricles to fill up with blood. Next, the electrical impulse travels to the bundle of His located in the interventricular septum and divides into the right and left bundle branches where it rapidly spreads through the purkinje fibers to the muscles of the right and left ventricle, causing them to depolarize and contract at the same time. Therefore, it can be said that a natural heart contracting impulse travels quickly to all portions of the ventricles, producing a synchronous contraction. This is the natural synchronization of the heart.
AAI leads are known to preserve both atrial ventricular synchronization and the normal ventricular activation and contraction patterns. However, AAI pacing is ineffective in correcting for a damaged AV node or a damaged right/left bundle branch block such as in second or third degree heart block. Presently only ventricular pacing has proved capable of resolving acute problems such as atrioventricular (AV) block or right/left bundle branch block. In ventricular pacing, a voltage pulse typically of 1 Volt/centimeter field strength is used to contract the muscle of the heart. However, ventricular pacing operates somewhat counter to the heart's natural operation. When an electrode located in the apex of the right ventricle delivers the electrical pulse, the myocyte cells local to the apex begin to contract. The electrical signal then expands relatively slowly, compared to the heart's natural contraction, upward and outward until the ventricles fully contract. Therefore, in ventricular pacing the electrical signal travels vertically and laterally from the bottom to the top of the ventricles. This is quite obviously not the heart's natural contraction pattern. Some studies have shown that ventricular pacing not only remodels the heart but this remodeling is associated with congestive heart failure.
Further, some studies have put forth the proposition that significant problems are associated with ventricle pacing. These studies have alleged that, while DDD pacing still preserves atrial ventricular synchronization, it will disrupt ventricular activation and contraction patterns. Moreover, these studies have also alleged that VVI pacing disrupts both atrial ventricular synchronization and ventricular activation and contraction. These studies propose that there is excess mortality in patients receiving ventricular stimulation when compared to stimulation in the upper atrial wall. It has been speculated that this excess mortality is due to heart damage caused by pacing the ventricular apex.
In addition to the problems mentioned above, it has been speculated that ventricular pacing can cause ventricular wall abnormalities due to asynchronous activation and can alter the ventricle volumes. It is speculated that VVI pacing causes heart failure and decreases left ventricular function when compared with AAI pacing. Further, some speculate that DDD chronic ventricular pacing causes a reduced inferior, septum, and global mean myocardial blood flow as well as a decreased left ventricular ejection fraction. These problems are suspected as being due to a reduction in the regional myocardial blood flow. Moreover, several studies have speculated that pacing the right ventricular apex causes these inferior localized myocardial perfusion defects and mitral regurgitation.
Another significant problem is that both DDD and VVI pacing have been alleged to create myofibrilar disarray and fatty deposits throughout the ventricles. Myofibrilar disarray and fatty deposits have been associated with congestive heart failure.
Therefore, what is clearly needed is a method and apparatus for providing atrial ventricular synchronization and proper ventricular activation and contraction for heart patients having AV nodal block, right or left bundle branch block, and in certain circumstances where the heart's intrinsic conduction system is in tact, heart failure. In addition, what is clearly needed is a method and apparatus to prevent remolding of the heart. Further, what is clearly needed is a method and apparatus to prevent inferior myocardial perfusion defects and mitral regurgitation.